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The chemomodulatory effects of resveratrol and didox on herceptin cytotoxicity in breast cancer cell lines
Herceptin is considered an essential treatment option for double negative breast cancer. Resveratrol and didox are known chemopreventive agents with potential anticancer properties. The aim of the current study is to investigate the influence of resveratrol and didox on the cytotoxicity profile of h...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4496837/ https://www.ncbi.nlm.nih.gov/pubmed/26156237 http://dx.doi.org/10.1038/srep12054 |
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author | Abdel-Latif, Ghada A. Al-Abd, Ahmed M. Tadros, Mariane G. Al-Abbasi, Fahad A. Khalifa, Amany E. Abdel-Naim, Ashraf B. |
author_facet | Abdel-Latif, Ghada A. Al-Abd, Ahmed M. Tadros, Mariane G. Al-Abbasi, Fahad A. Khalifa, Amany E. Abdel-Naim, Ashraf B. |
author_sort | Abdel-Latif, Ghada A. |
collection | PubMed |
description | Herceptin is considered an essential treatment option for double negative breast cancer. Resveratrol and didox are known chemopreventive agents with potential anticancer properties. The aim of the current study is to investigate the influence of resveratrol and didox on the cytotoxicity profile of herceptin in HER-2 receptor positive and HER-2 receptor negative breast cancer cell lines (T47D and MCF-7 cell lines, respectively). The IC(50)’s of herceptin in T47D and MCF-7 were 0.133 ± 0.005 ng/ml and 23.3795 ± 1.99 ng/ml respectively. Equitoxic combination of herceptin with resveratrol or didox in T47D significantly reduced the IC(50) to 0.052 ± 0.001 and 0.0365 ± 0.001 ng/ml, respectively and similar results were obtained in MCF-7. The gene expression of BCL-xl was markedly decreased in T47D cells following treatment with herceptin/resveratrol compared to herceptin alone. Immunocytochemical staining of HER-2 receptor in T47D cells showed a significant reduction after treatment with herceptin/resveratrol combination compared to herceptin alone. On the contrary, herceptin/didox combination had no significant effect on HER-2 receptor expression. Cell cycle analysis showed an arrest at G2/M phase for both cell lines following all treatments. In conclusion, herceptin/resveratrol and herceptin/didox combinations improved the cytotoxic profile of herceptin in both T47D and MCF-7 breast cancer cell lines. |
format | Online Article Text |
id | pubmed-4496837 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-44968372015-07-13 The chemomodulatory effects of resveratrol and didox on herceptin cytotoxicity in breast cancer cell lines Abdel-Latif, Ghada A. Al-Abd, Ahmed M. Tadros, Mariane G. Al-Abbasi, Fahad A. Khalifa, Amany E. Abdel-Naim, Ashraf B. Sci Rep Article Herceptin is considered an essential treatment option for double negative breast cancer. Resveratrol and didox are known chemopreventive agents with potential anticancer properties. The aim of the current study is to investigate the influence of resveratrol and didox on the cytotoxicity profile of herceptin in HER-2 receptor positive and HER-2 receptor negative breast cancer cell lines (T47D and MCF-7 cell lines, respectively). The IC(50)’s of herceptin in T47D and MCF-7 were 0.133 ± 0.005 ng/ml and 23.3795 ± 1.99 ng/ml respectively. Equitoxic combination of herceptin with resveratrol or didox in T47D significantly reduced the IC(50) to 0.052 ± 0.001 and 0.0365 ± 0.001 ng/ml, respectively and similar results were obtained in MCF-7. The gene expression of BCL-xl was markedly decreased in T47D cells following treatment with herceptin/resveratrol compared to herceptin alone. Immunocytochemical staining of HER-2 receptor in T47D cells showed a significant reduction after treatment with herceptin/resveratrol combination compared to herceptin alone. On the contrary, herceptin/didox combination had no significant effect on HER-2 receptor expression. Cell cycle analysis showed an arrest at G2/M phase for both cell lines following all treatments. In conclusion, herceptin/resveratrol and herceptin/didox combinations improved the cytotoxic profile of herceptin in both T47D and MCF-7 breast cancer cell lines. Nature Publishing Group 2015-07-09 /pmc/articles/PMC4496837/ /pubmed/26156237 http://dx.doi.org/10.1038/srep12054 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Abdel-Latif, Ghada A. Al-Abd, Ahmed M. Tadros, Mariane G. Al-Abbasi, Fahad A. Khalifa, Amany E. Abdel-Naim, Ashraf B. The chemomodulatory effects of resveratrol and didox on herceptin cytotoxicity in breast cancer cell lines |
title | The chemomodulatory effects of resveratrol and didox on herceptin cytotoxicity in breast cancer cell lines |
title_full | The chemomodulatory effects of resveratrol and didox on herceptin cytotoxicity in breast cancer cell lines |
title_fullStr | The chemomodulatory effects of resveratrol and didox on herceptin cytotoxicity in breast cancer cell lines |
title_full_unstemmed | The chemomodulatory effects of resveratrol and didox on herceptin cytotoxicity in breast cancer cell lines |
title_short | The chemomodulatory effects of resveratrol and didox on herceptin cytotoxicity in breast cancer cell lines |
title_sort | chemomodulatory effects of resveratrol and didox on herceptin cytotoxicity in breast cancer cell lines |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4496837/ https://www.ncbi.nlm.nih.gov/pubmed/26156237 http://dx.doi.org/10.1038/srep12054 |
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